viral meningitis
Introduction
Introduction to viral meningitis Both viral encephalitis (viralencephalitis) and viral meningitis (viral meningitis) refer to acute intracranial inflammation caused by various viruses. Due to the pathogenicity of pathogens and differences in host response processes, different types of diseases are formed, if the inflammatory process is mainly The meninges are clinically characterized by viral meningitis. Viral encephalitis is a clinical feature when it mainly affects the brain parenchyma. Most patients have a self-limiting course of disease. Viral meningitis (virusmeningitis) was called aseptic meningitis around the 1950s, probably because patients had typical meningeal irritation and cerebrospinal fluid examination using smear and culture methods could not find bacteria and Fungi, pathological changes are similar to viral infections. basic knowledge The proportion of illness: 0.035% Susceptible people: good for children Mode of infection: respiratory transmission Complications: disturbance of consciousness cerebral palsy
Cause
Cause of viral meningitis
(1) Causes of the disease
With the development of virological research, especially tissue cell culture, blood and cerebrospinal fluid infection pathogen detection technology, it is now clear that most of the disease is enterovirus infection, followed by mumps virus and lymphocytic choriomeningitis virus. A small number of herpes viruses include herpes simplex virus and varicella zoster virus.
In addition, viruses such as Epstein-Barr virus (EBV) and cytomegalovirus can cause this disease.
Enterovirus is the smallest non-coated RNA virus that can survive in sewage for a long period of time. Human beings are the natural host of enterovirus. Once enterovirus enters the body, it can enter the cell cytoplasm and destroy and kill. Cells, enteroviruses are generally divided into three types, namely poliovirus, coxsackievirus and ECHO virus, in addition to the unclassified enterovirus, and these There are many subtypes of enteroviruses, such as Coxsackie virus type A and B, but both types can cause viral meningitis, and can even cause encephalitis and acute cerebellar ataxia, Echovirus It can be isolated by cell culture in normal feces, and generally does not cause disease. Echovirus has more than 30 serotypes.
(two) pathogenesis
The virus enters the lymphatic system through the intestine (such as enterovirus) or the respiratory tract (such as adenovirus and rash), and then infects some organs outside the skull through the bloodstream (the arbovirus directly enters the bloodstream). The patient may have systemic symptoms such as fever, enter the central nervous system in the late stage of viremia, and enter the cerebrospinal fluid through the choroid plexus, which may cause central nervous system symptoms. If the host has a strong immune response to the viral antigen, it will further lead to demyelination, blood vessels and Perivascular brain tissue damage.
The virus can also cause myocarditis, pharyngitis, intercostal muscle pain and skin damage in the human body.
Most of the pathological changes are diffusely distributed, but they can also be prominent in some brain regions, showing a relatively limited tendency.
There are no abnormalities in the general observation of the brain. The cerebral surface is filled with blood vessels and cerebral edema. The meninges and/or brain parenchyma are extensively hyperemic, edematous, with lymphocytes and plasma cells infiltrating. The lesions are mainly in the pia mater. See arachnoid infiltration of monocytes, vascular sheath formed by infiltration of perivascular inflammatory cells in the superficial layer of the brain, degeneration of nerve cells around the perivascular tissue, necrosis and disintegration of myelin, but no inflammatory changes and nerves in deep brain and spinal cord tissue Evidence of cell necrosis.
In some patients with encephalitis, the pathological manifestations of demyelination are clearly seen, but the related neurons and axons are relatively intact. This pathological feature represents the immune response elicited by viral infection, suggesting "post-infection" or "allergic" "The pathological features of encephalitis.
Prevention
Viral meningitis prevention
Prevention: Usually exercise more, improve disease resistance, prevent colds and intestinal infections, and prevent them from getting worse once they are treated promptly and effectively. Vaccination against measles, rubella, mumps, etc.; anti-mosquito, anti-mosquito, vaccination against Japanese encephalitis vaccine.
Viral encephalitis is not contagious, and early symptoms are similar to colds and are easily overlooked by patients.
1. Pay attention to enhance physical fitness and prevent upper respiratory tract infections.
2. Newborns and children actively implement planned immunization as required.
3. Early comprehensive treatment to reduce complications and sequelae.
Complication
Viral meningitis complications Complications, consciousness, cerebral palsy
1. Consciousness of consciousness, even to the cortical state and other varying degrees of consciousness change.
2. Symptoms of increased intracranial pressure, if the respiratory rhythm is irregular or the pupil is not equal, consider the possibility of intracranial hypertension and cerebral palsy.
3. Most of the complete recovery, but a few left behind epilepsy, limb paralysis, intelligent developmental delay and other sequelae.
Symptom
Viral meningitis symptoms Common symptoms Irritability, convulsions, diarrhea, single stun, involuntary movement, nausea, abdominal pain, illusion, lethargy
Viral meningitis caused by Coxsackie virus or Echovirus, clinical manifestations are similar, infants, children and adults can be sick, acute or subacute onset, fever, headache, nausea, vomiting, abdominal pain, diarrhea , sore throat, general weakness, rapid neck stiffness and typical meningeal irritation such as Kernig sign positive, severe cases may appear symptoms of nervous system damage such as drowsiness, a small number of patients with lip herpes should consider whether it is herpes virus As a result, those with enlarged parotid glands should consider the possibility of mumps virus infection.
The severity of the disease varies greatly depending on the lesion mainly in the meninges or brain parenchyma. Generally speaking, the clinical course of viral encephalitis is more serious than meningitis, and severe encephalitis is more likely to cause acute death or sequelae.
1. Acute onset of viral meningitis, or first-infected or pre-infectious infectious diseases, mainly characterized by fever, nausea, vomiting, weakness, lethargy, older children will complain of headaches, babies are restless, irritating, There are usually few severe disturbances of consciousness and convulsions. There may be signs of meningeal irritation such as neck stiffness, but there are no localized signs of the nervous system. The course of the disease is mostly 1 to 2 weeks.
2. Viral encephalitis is an acute onset, but its clinical manifestations vary depending on the location, extent and severity of the main pathological changes. The course of viral encephalitis is mostly 2 to 3 weeks.
(1) Most children are mainly characterized by fever, recurrent seizures, varying degrees of disturbance of consciousness and increased intracranial pressure on the basis of diffuse cerebral lesions. Most of the convulsions are full, but there may be focal seizures. In a state of horror and persistent state, the child may have different levels of consciousness changes such as lethargy, lethargy, coma, deep coma, and even cortical state. If the respiratory rhythm is irregular or the pupil is not large, the possibility of intracranial hypertension and cerebral palsy may be considered. Some children are still with hemiplegia or limb paralysis.
(2) Some children mainly involve the frontal cortex motor area, and the clinical manifestations are repeated convulsions with or without fever, most of which are all or focal tonic-clonic or clonic seizures. A small number of manifestations of myoclonus or tonic seizures can occur in the epileptic seizure state.
(3) If the brain lesions mainly involve the bottom of the frontal lobe, the marginal system of the temporal lobe, the patient is mainly characterized by mental and emotional abnormalities such as mania, hallucinations, aphasia and orientation, computational power and memory impairment, with or without fever. A variety of viruses can cause such manifestations, but the most common cause is herpes simplex virus. The inclusions containing viral antigen particles are easily seen in the nerve cells of the virus encephalitis, sometimes called acute inclusion body encephalitis, often combined. Convulsions and coma, high mortality.
Others include hemiplegia, single sputum, quadriplegia or various involuntary movements. Many patients may have multiple types of manifestations at the same time. Positive pathological signs appear when the lesion involves the pyramidal tract.
Examine
Examination of viral meningitis
1. The surrounding white blood cell count is normal or slightly elevated.
2. The appearance of cerebrospinal fluid examination is colorless and transparent, the pressure is normal or slightly higher, and the white blood cells are mild to moderately elevated. Generally, it is (25-250)×106/L. The neutral multinucleated white blood cells are mainly within 48 hours after the onset, but quickly change to Mononuclear cells predominate, proteins are slightly increased, sugars are normal, chlorides are reduced, and no bacteriophage is found in smears and cultures.
3. The virological examination of some children with cerebrospinal fluid virus culture and specific antibody test positive, the recovery period serum specific antibody titer is more than 4 times higher than the acute phase has diagnostic value.
4. Imaging examination CT or MRI in the brain is generally normal.
5. EEG is characterized by diffuse or localized abnormal slow-wave background activity, a few with spikes, slow-synchronous waves, slow-wave background activity can only suggest abnormal brain function, can not confirm the nature of viral infection, some patients The EEG is also normal.
Diagnosis
Diagnosis and identification of viral meningitis
Diagnostic criteria
The diagnosis of most viral meningitis or encephalitis depends on the elimination of other non-viral infections in the brain, and the establishment of common acute brain diseases such as Reye syndrome.
A small number of patients who are explicitly concurrent with a viral infection, or cerebrospinal fluid examination confirmed that the specific virus antibody is positive, can directly support the diagnosis of intracranial viral infection.
According to the clinical onset, the onset is relatively rapid, with fever, headache, and meningeal irritation, CSF examination is colorless and transparent, white blood cells are mild, moderately increased, and monocytes are mainly changed, if the patient lacks brain damage The evidence is not difficult to consider as viral meningitis, but it is not easy to completely rule out viral encephalitis only in clinical manifestations, especially in severe cases, people with mental disorders and convulsions, even if brain imaging examination suggests brain mass and It is difficult to completely eliminate without damage.
In the past, in the diagnosis of pathogens, more blood, CSF, throat swabs for virus cell culture and isolation, but the time and the positive rate is not ideal, the current use of serological detection of Coxsackie, Echo and herpes simplex and other viruses When an antibody is diagnosed, a positive result must be detected several days after the onset of the disease, and the antibody can be present in the blood for several weeks. The detection of the virus by polymerase chain reaction (PCR) technique from CSF or blood can also help to diagnose the pathogen.
Differential diagnosis
The incidence of summer and autumn should be differentiated from Japanese encephalitis. The latter brain CT or MRI has more basal nucleus lesions. Patients with sporadic cases are different from herpes simplex encephalitis. Brain CT and MRI often show significant damage to the ventral surface of the temporal lobe and frontal lobe. In addition, it is necessary to identify with tuberculous meningitis, fungal meningitis, syphilitic meningitis and bacterial meningitis.
1. Other pathogen infections in the cranium are mainly based on the appearance of cerebrospinal fluid, routine, biochemical and pathogenic examination, and identification of purulent, tuberculous, cryptococcal meningitis. In addition, patients with subdural effusion support infantile purulent meningitis and found Extracranial tuberculosis lesions and skin PPD positive can help diagnose tuberculous meningitis.
2.Reye syndrome is complicated by the symptoms of acute encephalopathy and no obvious abnormalities of cerebrospinal fluid. However, according to Reye syndrome, there is no obvious jaundice and liver function is abnormal. 3 to 5 days after onset, the condition no longer progresses, and some patients have blood sugar. Reduced and other characteristics, can be identified with viral meningitis or encephalitis.
